Aphasia - Sydney Cognitive Development Centre

(1) Broca’s Aphasia

Aphasia can follow any type of neuropathology
capable of causing structural alterations in the
language area of the brain. It is the
neuroanatomical site of damage, rather than the
etiology, that determines the individual symptoms of
language impairment. In Broca’s aphasia left
hemisphere damage of the anterior part of the peri-
Sylvian language zone involving the third frontal
convolution (i.e., Broca’s Area) is often found.
However, much controversy exists over the exact
location of the lesion necessary to result in this
aphasia. For example, there is evidence that Broca’
s aphasia may arise from a lesion in the lenticular
zone, anterior portions of the insular cortex,
precentral gyrus, or lesions in the fibers of both the
corpus callosum and the left internal capsule (see
Levine and Sweet, 1983, for a review). Different
types of neuropathology may be involved in this
aphasia. For example, a CVA in the orbitofrontal
branch of the middle cerebral artery is a possible
aetiology, as well as trauma such as an open- or
closed-head injury resulting in damage to the
specific areas described above. Likewise a tumor
may also produce the aphasia by growing in the
specific regions, by increasing intercranial pressure,
or by disrupting blood supply. Similarly, infectious
diseases can also build up cranial pressure and
result in damage to the language areas.
Degenerative disorders may also be involved if the
atrophy extends to the language areas.

Broca’s aphasia is also known as an expressive or
non-fluent aphasia, and is predominantly a motor
aphasia. The manifestations of this syndrome are
awkward articulation, restricted vocabulary,
restriction of grammar to the simplest, most over
learned forms, and abnormal prosody. However,
there is relative preservation of auditory
comprehension. There is also an awkwardness and
distortion of phonemes including literal paraphasias.
Output often contains an excess of semantically
significant words with a reduction or absence of
syntactical structures or affixes. Although
comprehension of spoken language is better than
verbal output, comprehension is rarely normal,
particularly in regard to grammatically significant
structures. Repetition of spoken language is also
abnormal. Naming is poor but may be aided by
contextual or phonetic prompting. In addition,
omissions, iterations, and simplifications of syllabic
clusters often occur. These types of deficits are also
evident in written language and reading outloud,
however, reading comprehension is not
impaired.

Broca’s aphasia causes significant problems for its
sufferers. Firstly, the abrupt loss of language will
severely jeopardize the stability of the patients
existence in areas such as work, social life, and
relationships. The rich substantive output enables
one with this aphasia to communicate ideas,
however, in general communication will be very
poor. Secondly, some time after onset of the
disorder most nonfluent aphasic patients become
aware of their problems. They often know what to
say but have a verbal output that is restricted and
barely intelligible. The inability to explain wishes or
thoughts is frustrating for the patient, and many
patients with nonfluent aphasia suffer both
frustration and depression. Patients often may show
lack of interest and motivation and a helpless
attitude and suicidal thoughts may occur (Benson &
Ardilla, 1996).

The prognosis of Broca’s aphasia depends on
several factors. Like most aphasias there will be an
early spontaneous recovery stage. Patients often
respond automatically to their language problem by
developing alternate successful strategies for
communication. Several neurological factors are
crucial to the prognosis. Generally the greater the
lesion the worse the prognosis for recovery.
Patients with damage to adjacent areas to Broca’s
area, especially the inferior portion of the precentral
gyrus and anterior parietal region have a poorer
prognosis than those in whom the areas are spared.
Broca’s aphasia tends to improve in either two ways.
Firstly, in some cases sentence length and syntax
improve along with normalisation of articulation,
phonemic production and repetition (i.e., to
extrasylvian motor aphasia and then to anomic
aphasia). In other cases, sentence length and
syntax recovers without improved articulation,
phonemic production, and repetition (i.e., to a
conduction aphasia) (Benson & Ardilla, 1996).
Obviously one of the greatest factors which
influences prognosis is that of etiology. Progressive
disorders will result in deteriorating language
functions, whereas acute-onset, static disorders (e.
g., CVAs, trauma, and tumors) will have a better
potential for recovery. Trauma and hematoma
cases recover better than CVAs or tumors (although
this may be due to age influences). Most
intracerebral tumors have a poor prognosis,
whereas extracerebral tumors generally have a
good prognosis. These prognostic factors are
evident in all types of aphasia, not just Broca’s
aphasia (Sarno, 1981).

(2) Wernicke’s Aphasia

This aphasia generally arises from damage to the
posterior part of the peri-Sylvian language area,
usually a lesion involving the posterior superior
portion of the temporal lobe of the dominant
hemisphere (i.e., Wernicke’s area). This damage
may extend into the supramarginal/angular gyrus
region and/or the lateral-temporal-occipital junction
area. Again there is much controversy in the
literature on the exact localisation of the necessary
lesion. For example in some cases the anterior
prerolandic areas, temporal isthmus, anterior
portion of the putamen, and even Broca’s area has
been implicated (see Kertesz, 1983 for a review).
Like Broca’s aphasia it is the localisation of the
lesion that results in the syndrome rather than a
specific etiology. However, this disorder commonly
arises from left hemisphere strokes from blockages
or hemorrhages of the left tempero-parietal region.
Direct injury from closed head or open head wounds
are possible, as well as tumors, degenerative
disorders (e.g., Alzheimer’s disease), and infectious
diseases, as long as the infarcts occur in the
specified areas.

This syndrome manifests itself as an impairment in
auditory comprehension, and fluently articulated but
paraphasic speech. The impairment of
comprehension can even be evident at the single
word level. The paraphasia may include literal
paraphasia, verbal paraphasia, and neologisms.
Further symptoms include word-finding difficulties as
well as severe impairments in reading and writing.
Verbal output is fluent with a normal number of
words per minute. Patients often augment their
verbal output adding additional syllables to the ends
of words, or additional words at the end of
sentences. Little effort is needed for verbal output
and often the output is excessive. No problems exist
with articulation, or prosody, however, there is
sometimes an excessive use of grammar
(paragrammatism). Reading both outloud and for
comprehension, as well as writing are all often
disturbed. What characterizes Wernicke’s aphasia is
that the verbal output is often deficient in meaning
and is often termed “empty speech”.

Patients with Wernicke’s aphasia or a nonfluent
aphasia often have different problems compared to
those with a nonfluent aphasia. They not only have
difficulties in comprehending spoken language but
also often remain unaware of their comprehension
problem. This produces a true anosognosia. Many
patients cannot monitor their own verbal outputs
and therefore fail to realise their output is
incomprehensible. Patients also tend to blame their
communication difficulties on others, complaining
that the person they are talking to is not speaking
clearly. Patients also have difficulties in doing simple
everyday activities such as reading the newspaper
and watching television. Clearly disorders of
comprehension will affect relationships and make it
extremely difficult to be productive in most jobs. In
addition, since aphasia involves loss of braining
functioning due to lesions, the patient’s ability to
monitor, manage, and control cognitive operations
tends to be decreased. Thus, the brain injury may
also produce alterations in personality and mental
competence (Sarno, 1981).

In Wernicke’s aphasia poor prognosis has been
correlated with middle temporal gyrus,
supramarginal gyrus, postcentral gyrus, temporal
isthmus or insula involvement. This aphasia may
recover along two paths. Firstly, there may be better
auditory comprehension and improvement in
phonemic accuracy and repetition (i.e., toward
anomic aphasia). Secondly, there may be better
comprehension but poor repetition (i.e., toward
conduction aphasia). Prognosis also depends on
other factors previously described, such as the size
of the lesion and the types of etiology of the
aphasia.